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PAtho > Unit 6 and Unit 7 Part 1 > Flashcards

Unit 6 and Unit 7 Part 1 Flashcards

1
Q

influenza

A

acute viral infc in URT

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2
Q

when does influenza increase

A

seasonal infc

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3
Q

which types of influenza have inc prevelance

A

types A, B,C

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4
Q

incubation period for influenza

A

1-4 days

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5
Q

what strain of influenza usually causes epidemics

A

A

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6
Q

who has inc risk for influenza

A

HCP
peds pts
geri pts

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7
Q

why do HCP have inc risk for influenza

A

personally compromised rt repeat exposure

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8
Q

why do peds pts have inc risk for influ

A

defenses arent fully established yet

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9
Q

why do geri pts have inc risk for influ

A

dec defenses rt to age

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10
Q

patho influenza

A

viral injury to epithelial cells in URT, inflm/tissue damage

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11
Q

why may abx be perscribed in influ

A

prophylaxis ONLY, to dec risk of 2ndary infc rt compromised IR in pts w inc susceptibility

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12
Q

2 complications assoc with influ

A

2ndary bact infc

bronchitis/pnumonia

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13
Q

what are complications of influ rt to

A

movement of virus to LRT lt bronchial/alveolar damage

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14
Q

mnfts

A

cough
fever
malaise

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15
Q

characteristics of cough in influ

A

beneficial unless the URT is irritated, then it inc irritation/infc -> damage

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16
Q

course of influenza

A

self limiting

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17
Q

tx of influenza

A 
prevent spread
vaccine for prophylaxis
symptomatic mgmt
limit infc to urt
antivirals??
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18
Q

egs of antivirals

A

amantadine

rienza

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19
Q

amantadine

A

1st gen antiviral that inhibits RNA coating of virus

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20
Q

what strains is amantadine most effective against

A

A and B

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21
Q

rienza

A

2nd gen antiviral that inhibits replication of virus, prevents virus rls from host

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22
Q

pnuemonia

A

inflm of bronchioles and alveoli

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23
Q

what forms does pnuemonia come in

A

infectous

non infectous

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24
Q

what is pnuemonia classifed by

A

agent

location

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25
Q

et of pnuemonia

A

usually dt bact, or virus, fuingu
aspiration
inhalation of fumes

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26
Q

how does inflm occur in pnuemonia

A

agent enters RT and proceeds into lungs

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27
Q

why is it abn for an infectous agent to proceed into the lungs

A

pulmonary defense is impaired and cant filter out pathogens

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28
Q

what happens when there is inflm in the lungs in pnuemonia

A

pulm edema -> impaired gas exch -> Co2 build up -> systemic hypoxia

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29
Q

typical pnuemonai

A

bacterial pnuemonia that occurs where there is empty spaces

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30
Q

atypical pnuemonia

A

dt any other agent, virus? things proliferating using cells around tissues

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31
Q

lobar pnuemonia

A

lung inflm specific to an entire lobe

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32
Q

broncho pnuemonia

A

inflm throughout alveoli in entire lung

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33
Q

area of consolodation

A

area with solidification of 3 components

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34
Q

what 3 components make up areas of consolodation when solidified

A

exudate
inflm debris
inflm cells

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35
Q

how are areas of consolidation seen

A

on cxr

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36
Q

mnfts of pnuemonia

A 
fever/chills
dyspnea rt dec gas exchnage
sputum
headace
chest pain
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37
Q

what mnft makes pnuemonia different the flu

A

chest pain

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38
Q

sputum

A

combination of mucous and exudate

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39
Q

dx for pnuemonia

A

hx, px
cxr
sputum c and s

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40
Q

why are sputum c and s’s done in pnuemonia

A

to determine if abx are needed

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41
Q

tx of pnuemonia

A

abx with typical pnuemonia

symptomatic mgmt

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42
Q

COPD

A

persistant inflm causing aw, vasculature and parenchyma inflm

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43
Q

what episodic problem is prominent in copd

A

acute, recurrent, chronic obstr of aw

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44
Q

what disorder are included in copd

A

chronic bronchitis

emphysema

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45
Q

what may copd coexist with

A

aasthma

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46
Q

et/risks for copd

A

smoking (80-90%)
recurrent resp infc (not chronic)
aging
genetic def of alpha one antitrypsin

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47
Q

why does aging inc risk for copd

A

lt dec lung compliance rt age of aw and l/o elasticity

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48
Q

what does smoking do to mucous prod? what does it lead to

A

inc mucous in RT, lumenal obstr

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49
Q

how does smoking compromise the mucociliary blanket

A

destroys cilia that lines the RT

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50
Q

how does inc mucous in RT affect cilia

A

overwhelms them by mucous logging them

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51
Q

what does smoking do to the airway

A

inflames it

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52
Q

what effect does smoking produce? (mnft)

A

coughing

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53
Q

what does coughing do to the airway of the copd pt

A

inc damage to inflamed area

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54
Q

what structures of the RT does smoking destroy

A

aw

alveoli wall

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55
Q

3 mechanisms of airflow in chronic bronchitis (CB)

A

hypertrophy of bronchial wall
inflm and mucous sec
damage to elastic tissue

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56
Q

hypertrophy of bronchial wall in CB

A

lt dec lumen size dt inc inflm

57
Q

inflm and mucous sec in CB

A

lt up to 50 percent lumen obstr. dt inflm causing inc exudate and smoking lt inc mucous

58
Q

damage to elastic tissue in CB

A

lt dec compliace, airway is no longer held open

59
Q

what is CB dt

A

smoking, reccurent infc

60
Q

where do changes in CB appear first

A

large aw

61
Q

characteristics of affected large aw in CB

A

hypertrophy of submucousal glands rt inc gland workload

62
Q

why do submucosal glands of inc workload in CB

A

dt inc sec of mucous dt smoking

63
Q

where do changes appear second in CB

A

smaller airway

64
Q

what changes occur in the smaller aw in CB

A

inc in goblet cells

65
Q

what does inc/excess mucous in CB lt

A

impaired mucociliary defense

66
Q

what happens when mucociliary defenses are compromised in CB

A

infc and bronchial wall inflm

67
Q

why does aw collapse occur in the patho of CB

A

lumen obstr rt inflm leads to collapse caused by trapping of air in terminal aw. air slowly diffuses out into circulation lt collapse

68
Q

what happens do alveolar ventilation in CB, why

A

decreases, dt air trapped in parts of lung

69
Q

what happens when there is a V:P imbal

A

hypoxemia

70
Q

hypoxemia

A

dec O2 in ABG

71
Q

V in V:P

A

air moving in and out lungs

72
Q

P in V:P

A

gaseous exchange

73
Q

normal V:P

A

0.8

74
Q

normal V

A

4L air in and out/min

75
Q

normal P

A

5.5L blood thru PC /min

76
Q

what is important to remember about VP ratio

A

it could be the same number even if V and P are smaller, abn numbers

77
Q

what variable changes in CB

why

A

V

dt abn obstr. even though aw may collapse, its still a ventilation problem, not perfusion

78
Q

dx CB

A

chronic cough (cant use coughing alone)

79
Q

chronic cough

A

presence of cough for 3 consec mo for 2 years

80
Q

main mfnt of CB

A

impaired resp fx

81
Q

how is impaired resp evidenced by

A

hypoxemia

hypercapnia

82
Q

resp fx

A

composed of gas exch and ventilation

83
Q

other mnfts of CB (7)

A 
activity intol
inc mucous prod
sputum
dyspnea
wheezing w/o auscultation
wet crackles
inc expiratory length
84
Q

what is dyspnea in CB dt

A

lumen obstr

85
Q

what is wheezing dt in CB

A

thinning aw

86
Q

why are wet crackles heard in auscultation in CB

A

air moving over and thru mucous

87
Q

why is expiration length inc in CB

A

rt dec elastic recoil of lungs -> trouble compressing TC to exhale quickly

88
Q

complication of CB

A

secondary bact infc rt mucous accum

89
Q

emphysema

A

destr of alveolar tissue and capilarry beds

90
Q

what are of lung has inc incidence for emphysema

A

terminal airway

91
Q

what does emphysema lt

A

l/o compliance

92
Q

compliance

A

ease of lung filling/emptying with inc difficulty breathing

93
Q

what happens to distal airspace in alveoli in emphysema

A

increases dt loss of wall integerity

94
Q

what causes enlarged distal airspaces in emphysema

A

alveolar merging

95
Q

why is alveolar merging not beneficial

A

inc alveolar size -> inc SA -> dec surface for gas exchange

96
Q

et emphysema

A

smoking (classic)

genetic def of alpha1 antitrypsin (A1A)

97
Q

fx of A1A

A

protease, ez inhibitor, allows break down of old protein in an organized and controlled fashion

98
Q

what is A1A responsible for

A

regulating protein breakdown in lungs

99
Q

what does smoking do to A1A in classic emphysema

A

inhibits it

100
Q

what happens when a1a is inhibited

A

inflm and protein break down in lungs

101
Q

what does cigarette smoke attract to the lungs

A

inflm cells

102
Q

what do inflm cells bring to lungs

A

inc proteases

103
Q

what do proteases do to the lungs

A

alveolar damage

104
Q

how is smoking with classic emphysema a triple wammy in terms of patho and lung damage

A

inhibits inhibitor
increases inflm cells
inflm cells bring inc protease

105
Q

why is ventilation impaired in emphysema

A

permanent distended air spaces

106
Q

what VP variable does emphysema change

A

Both

107
Q

why is WoB inc in emphysema

A

air is trapped in spaces between alveoli

108
Q

what does trapped air result in

A

increased amount of dead space

109
Q

dead space

A

areas not involved in gas exchange

110
Q

why is ventilatory effort in emphysema increased

A

rt dec/compromised lung capacity

111
Q

what 3 things mean increased work of breathing

A

nasal flaring
pursed lip breathing
accessory m use

112
Q

why does the P variable change in emphysema

A

capillary walls are destroyed by proteases -> impaired perfusion

113
Q

another name for air pocket inbetween alveoli

A

bleb

114
Q

bullae

A

when a bleb inc in size and is visible bc it presses on plueral memb

115
Q

what does smoking lt (fig flowcart)

A

attraction of inflm cells

dec a1a activity

116
Q

what is released when inflm cells are attracted (fig flowchart)

A

elastase

117
Q

what inhibits the action of elastase (fig flowchart)

A

a1a

118
Q

what causes destruction of elastic fibers in lungs (fig flowchart)

A

dec a1a dt smoking
inherited a1a def
inhibited elastase action

119
Q

what does destruction of elastic fibers lead to in lungs (fig flowchart)

A

emphysema

120
Q

2 types of emphysema

A

centraacinar

panacinar

121
Q

centriacinar emphysema

A

destruction is confied to terminal and respiratory bronchi.

122
Q

alveoli condition in centriacinar emphysema

A

currently have little damange

123
Q

which type of emphysema is most common

A

centraacinar

124
Q

panacinar

A

damage to aw and peripheral alveoli

inc severity

125
Q

mfnts of emphysema

A

dyspnea
inc ventilatory effor
barrel chest

126
Q

what makes something a barrel chest

A

when chests transverse diameter and anterioposterior diameter are equal (2:2)

127
Q

what is a normal chest diamter ration

A

2:1 transverse to anterioposterior

128
Q

dx for COPD

A

hx, px
labs
cxr
pulm fx tests

129
Q

what do pulm fx tests measure

A

lung vol

130
Q

tx for COPD

A

limit progression
lifestyle mod
vaccine
drugs

131
Q

what lifestyle mods have to be made to tx copd

A

NO smoking

avoid aw irritants

132
Q

why do we encourage COPD pts to get vaccianted

A

for prophylaxis rt dec IR and inc susceptibility

133
Q

what vaccinations should copd pts receive

A

flu q1 year

pnuemonial q5year

134
Q

first line drugs for COPD

A

short acting b receptor agonist

anticholinergics

135
Q

what happens if first line drugs arent working for COPD

A

add inhaled steroids

136
Q

what do we do if a short acting b receptor agoinst isnt working COPD

A

long acting b receptor agonist

137
Q

thcophyline (COPD)

A

bronchodilator with some anti inflm properties

138
Q

how do beta receptors work

A

cause bronchodilation in bronchiols (smaller aw)

139
Q

how do anticholinergics work

A

cause bronchodilation in larger aw (bronchi)

PAtho (31 decks)

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